Ischemia/reperfusion injury in aging mouse hearts

University Of Arkansas Med Scis Ltl Rock, Little Rock AR

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Abstract

The process of aging adds significantly to the complexity of the mechanisms that are involved in mediating myocardial response to ischemic stress and to the subsequent deterioration of myocardial structure and function. Heart disease, especially congestive heart failure secondary to myocardial ischemia/infarction, increases in prevalence with advancing age and is the largest single cause of death in men and women over 65 years. It is important that the interactions of post- maturational cardiac aging and the superimposed response to myocardial stress be better understood. We need to know why heart failure after ischemia or ischemia/reperfusion develops more readily and the associated mortality and morbidity are so much higher in older age persons. Our recent observations suggest that in response to acute ischemia, the heart of the older animal is likely to sustain a larger infarct size and also more DNA fragmentation as compared to that of the young adult. We propose 2 specific aims: (1) To test the hypothesis that c jun NH-2- terminal kinase (JNK) activation induced by oxidative stress might mediate cell death and DNA fragmentation in cardiac myocytes; (2) To test the hypothesis that c-Jun NHZ-terminal kinase (JNK) may have a significant role in the age difference in the cardiac injury response to oxidative stress.